Studies of muscarinic m1, m3, or m5 receptor-mediated signal transduction demonstrated simultaneous stimulation of phospholipase A2, phospholipase C, Phospholipase D, adenylate cyclase, tyrosine kinase, and calcium influx. Calcium influx activation and tyrosine phosphorylation occurs transduction pathways. Muscarinic receptor-induced tyrosine phosphorylation was calcium influx dependent and resulted in the tyrosine phosphorylation of phospholipase-C-gamma. Muscarinic ml, m3, and m5 receptors induce a morphology change and have a tumor suppressor function when expressed in CHO cells. The morphology change was independent of all signal transduction pathways tested except receptor-operated calcium influx and tyrosine phosphorylation. Tyrosine phosphorylation was calcium influx dependent. Muscarinic receptors-operated calcium channel activation plays a central role in CHO cell tumorigenicity. Human and rat cannabinoid receptors expressed in CHO or L cells were linked to the inhibition of adenylate cyclase. Other Gi - coupled receptors linked to the inhibition of adenylate cyclase, such as alpha2, D2, M2, and m4 receptors were shown to augment ATP-stimulated phospholipase A2, but not the cannabinoid receptor. Cannabinoid receptor-activation had no effect on phospholipase A2, or C, although, high concentrations of cannabinoid agonists stimulated the release of arachidonic acid, intracellular calcium, and the inhibition of arachidonic acid uptake in a receptor-independent manner.